Muscle Cramps in Athletes: Causes and the Link to Training Load and Drugs

Almost every athlete has felt it: a calf that locks up in the final miles of a marathon, a hamstring that seizes during overtime, a foot that knots at night after a hard week. Exercise-associated muscle cramps are common, painful and still not fully explained. Our editorial team reviewed the main theories, the role of training load, and the medications and performance-enhancing substances that make cramps more likely.

What a cramp actually is

A muscle cramp is a sudden, involuntary and painful contraction of a muscle or part of a muscle, often with a visible or palpable knot. It typically lasts from a few seconds to several minutes and resolves with stretching. Exercise-associated muscle cramps (EAMC) occur during or shortly after physical activity, most often in muscles that cross two joints, such as the calves, hamstrings and quadriceps.

Electrical recordings show that cramps originate in the nervous system rather than the muscle fibers themselves. Motor neurons fire at high frequency, and the muscle cannot relax. This distinguishes true cramps from contractures seen in some metabolic muscle diseases, where the muscle is electrically silent.

Nocturnal leg cramps, which strike at rest, often at night, overlap with EAMC but are more common in older adults and in pregnancy. Athletes who train hard frequently report both kinds, particularly during heavy training blocks.

Most cramps are benign. Persistent cramps, cramps with weakness, dark urine, swelling or numbness, or cramps unrelated to exercise warrant medical evaluation, since they can signal electrolyte disorders, nerve problems, thyroid disease or muscle breakdown.

Fatigue versus dehydration: the two main theories

For decades, cramps were blamed on dehydration and salt loss. Sports drinks and salt tablets were marketed largely on that basis. The theory has intuitive appeal: heavy sweaters lose a lot of sodium, and cramps are common in hot conditions.

The competing "altered neuromuscular control" theory, championed by Schwellnus, argues that fatigue disrupts the balance between excitatory signals from muscle spindles and inhibitory signals from Golgi tendon organs. When the muscle is fatigued and contracting in a shortened position, the spinal reflex loop becomes over-excited and a cramp results.

Prospective evidence supports the fatigue model. In a cohort of 196 Ironman triathletes, Schwellnus and colleagues found that athletes who cramped did not differ in dehydration or serum sodium from those who did not. Instead, faster race pace relative to training and a history of previous cramps predicted cramping.

The two theories are not mutually exclusive. Bergeron described a subset of athletes, often heavy, salty sweaters in American football or tennis, who develop widespread cramps in the heat that seem related to large sodium deficits. For most recreational athletes, however, cramps track with intensity and fatigue more than with fluid loss.

Training load and other risk factors

The single strongest predictor of future cramps is having had them before. Beyond that, the most consistent risk factors relate to load: racing faster or longer than you have trained for, sudden increases in volume, and insufficient recovery between hard sessions.

Muscles that work in shortened positions are particularly vulnerable. Swimmers cramp in the calves and feet when pointing their toes; cyclists cramp in the quadriceps and hamstrings during long climbs; sprinters and soccer players cramp in the hamstrings late in games.

• Inadequate conditioning for the event's demands
• Poor pacing, especially a fast start
• Heat, particularly in unacclimatized athletes
• Low carbohydrate availability and glycogen depletion
• Poor sleep and accumulated fatigue
• Very high sweat sodium losses in some individuals

Addressing these factors, through gradual progression, event-specific training, sensible pacing and heat acclimatization, is the most evidence-based way to reduce cramping.

Medications and performance drugs that raise cramp risk

Several prescription drugs list cramps as a side effect. Diuretics deplete potassium and magnesium; statins can cause muscle pain and cramps; beta-2 agonists used for asthma can lower blood potassium; and some blood pressure drugs and osteoporosis medications have also been implicated.

In physique sports, the misuse of diuretics before competition to "dry out" is a well-documented cause of severe cramps, dangerous electrolyte disturbances and heart rhythm problems. Diuretics are also prohibited under the WADA Code as masking agents.

Clenbuterol, a beta-2 agonist not approved for human use in the US, is misused for fat loss. It can cause tremor, tachycardia, low potassium and painful cramps, and case reports describe cardiac complications. Thyroid hormone misuse, stimulants and high-dose caffeine can increase muscle excitability as well. Insulin misuse can drive potassium into cells and cause hypokalemia along with potentially fatal hypoglycemia.

If cramps begin after starting any new medication or substance, that link should be reported to a physician rather than managed with more electrolytes.

What helps during and after a cramp

The fastest relief comes from gentle passive stretching of the cramping muscle, for example pulling the toes toward the shin for a calf cramp. Stretching activates inhibitory reflexes and usually ends the cramp within seconds to a minute.

Small volumes of pickle juice have been shown to shorten electrically induced cramps. Miller and colleagues found that this happened too quickly to be explained by fluid or electrolyte absorption, suggesting a reflex triggered in the mouth or throat. Products based on strong flavors such as vinegar or capsaicin build on this idea, though evidence remains limited.

Magnesium supplements are widely used, but a Cochrane review found them unlikely to help typical nocturnal leg cramps in older adults. Quinine, once commonly prescribed, is not recommended; the FDA has warned against using it for leg cramps because of serious blood and heart side effects. A Neurology evidence review by Katzberg and colleagues reached similar conclusions about quinine's risk–benefit balance.

For prevention, regular stretching, strength training of cramp-prone muscles, better pacing and individualized hydration and sodium plans for heavy sweaters are reasonable strategies.

Conclusions of the Editorial Team

Most exercise-associated cramps reflect neuromuscular fatigue during unaccustomed effort, not simple dehydration. Better preparation and pacing usually help more than extra salt tablets.

Medications and performance drugs, especially diuretics, beta-2 agonists, stimulants and insulin, can provoke cramps through electrolyte shifts and carry serious risks beyond cramping. New or severe cramps after starting any substance deserve medical attention.

You might also be interested in our articles on hypokalemia in athletes, sodium needs for endurance events and the real risks of clenbuterol.

References

1. Schwellnus MP. Cause of exercise associated muscle cramps (EAMC)—altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med. 2009;43(6):401–408.
2. Schwellnus MP, Drew N, Collins M. Increased running speed and previous cramps rather than dehydration or serum sodium changes predict exercise-associated muscle cramping: a prospective cohort study in 196 Ironman triathletes. Br J Sports Med. 2011;45(8):650–656.
3. Bergeron MF. Muscle cramps during exercise: is it fatigue or electrolyte deficit? Curr Sports Med Rep. 2008;7(4):S50–S55.
4. Miller KC, Mack GW, Knight KL, et al. Reflex inhibition of electrically induced muscle cramps in hypohydrated humans. Med Sci Sports Exerc. 2010;42(5):953–961.
5. Katzberg HD, Khan AH, So YT. Assessment: symptomatic treatment for muscle cramps (an evidence-based review). Neurology. 2010;74(8):691–696.
6. Garrison SR, Korownyk CS, Kolber MR, et al. Magnesium for skeletal muscle cramps. Cochrane Database Syst Rev. 2020;9:CD009402.